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Alcoholic Hepatitis

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281. Controversies in Clinical Trials for Alcoholic Hepatitis. Full Text available with Trip Pro

Controversies in Clinical Trials for Alcoholic Hepatitis. Alcoholic hepatitis (AH) is the most severe form of alcoholic liver disease, contributing to significant morbidity and mortality. Yet, the only available therapies that improve survival are corticosteroids and liver transplantation, with no new drugs successfully developed for decades. This article briefly describes the current state of affairs in AH therapy and examines the practical and ethical challenges of conducting controlled (...) on a composite clinical endpoint that does not rely solely on mortality, as well as the adoption of the NIAAA Alcoholic Hepatitis Consortia recommendations regarding standard definitions and when to request a liver biopsy prior to study entry.Copyright © 2017 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

2017 Journal of Hepatology

282. Skeletal muscle mass to visceral fat area ratio is an important determinant affecting hepatic conditions of non-alcoholic fatty liver disease. (Abstract)

Skeletal muscle mass to visceral fat area ratio is an important determinant affecting hepatic conditions of non-alcoholic fatty liver disease. Not only obesity but also sarcopenia is associated with NAFLD. The influence of altered body composition on the pathophysiology of NAFLD has not been fully elucidated. The aim of this study is to determine whether skeletal muscle mass to visceral fat area ratio (SV ratio) affects NAFLD pathophysiology.A total of 472 subjects were enrolled

2017 Journal of gastroenterology

283. IL-1 receptor like 1 protects against alcoholic liver injury by limiting NF-κB activation in hepatic macrophages. Full Text available with Trip Pro

IL-1 receptor like 1 protects against alcoholic liver injury by limiting NF-κB activation in hepatic macrophages. Alcohol consumption increases intestinal permeability and causes damage to hepatocytes, leading to the release of pathogen- and damage-associated molecular pattern molecules (PAMPs and DAMPs), stimulating hepatic macrophages and activating NF-κB. The resultant inflammation exacerbates alcoholic liver disease (ALD). However, much less is known about the mechanisms attenuating (...) inflammation and preventing disease progression in most heavy drinkers. Interleukin (IL)-33 is a DAMP (alarmin) released from dead cells that acts through its receptor, IL-1 receptor like 1 (ST2). ST2 signaling has been reported to either stimulate or inhibit NF-κB activation. The role of IL-33/ST2 in ALD has not been studied.Serum levels of IL-33 and its decoy receptor, soluble ST2 (sST2) were measured in ALD patients. Alcohol-induced liver injury, inflammation and hepatic macrophage activation were

2017 Journal of Hepatology

284. Application of Prognostic Scores in The Stopah Trial: Discriminant Function is no Longer the Optimal Scoring System in Alcoholic Hepatitis. Full Text available with Trip Pro

Application of Prognostic Scores in The Stopah Trial: Discriminant Function is no Longer the Optimal Scoring System in Alcoholic Hepatitis. 'Static' prognostic models in alcoholic hepatitis, using data from a single time point, include the discriminant function (DF), Glasgow alcoholic hepatitis score (GAHS), the age, serum bilirubin, international normalized ratio and serum creatinine (ABIC) score and the model of end-stage liver disease (MELD). 'Dynamic' scores, incorporating evolution (...) = 0.02; GAHS 21% vs. 29.3%, p = 0.04). Overall mortality from treating all patients with a DF ≥32 and Lille assessment (90-day mortality 26.8%) was greater than combining newer 'static' and 'dynamic' scores (90-day mortality: MELD/Lille 21.8%; ABIC/Lille 23.7%; GAHS/Lille 20.6%).MELD, ABIC and GAHS are superior to the DF in alcoholic hepatitis. Consistently low scores have a favourable outcome not improved with prednisolone. Combined baseline 'static' and Day 7 scores reduce the number of patients

2017 Journal of Hepatology

285. Molecular Ellipticity of Circulating Albumin-Bilirubin Complex Associates With Mortality in Patients With Severe Alcoholic Hepatitis. Full Text available with Trip Pro

Molecular Ellipticity of Circulating Albumin-Bilirubin Complex Associates With Mortality in Patients With Severe Alcoholic Hepatitis. Hyperbilirubinemia and hypoalbuminemia are features of hepatic dysfunction that associate with disease severity. This is because hepatic insufficiency causes hypoalbuminemia, which indirectly increases the circulating levels of free bilirubin. Circular dichroism (CD) spectroscopy can be used to quantify the molecular ellipticity (ME) of the albumin-bilirubin (...) complex, and might associate with the severity or outcome of severe alcoholic hepatitis (SAH).We performed a cross-sectional study of 265 patients with SAH admitted in the Department of Hepatology, Institute of Liver and Biliary Sciences in New Delhi, India from January 2014 through January 2016. Blood samples were collected and patients were followed for 12 months or death. The molar ratios of bilirubin: albumin and albumin-bilirubin complexes were determined for a discovery cohort (30 patients who

2017 Clinical Gastroenterology and Hepatology

286. Extracorporeal Cellular Therapy (ELAD) in Severe Alcoholic Hepatitis - A Multinational, Prospective, Controlled, Randomized Trial. Full Text available with Trip Pro

Extracorporeal Cellular Therapy (ELAD) in Severe Alcoholic Hepatitis - A Multinational, Prospective, Controlled, Randomized Trial. Severe alcoholic hepatitis (sAH) is associated with a poor prognosis. There is no proven effective treatment for sAH, which is why early transplantation has been increasingly discussed. Hepatoblastoma-derived C3A cells express anti-inflammatory proteins and growth factors and were tested in an extracorporeal cellular therapy (ELAD) study to establish their effect

2017 Liver Transplantation Controlled trial quality: uncertain

287. Clinical Trial Design for Alcoholic Hepatitis. (Abstract)

Clinical Trial Design for Alcoholic Hepatitis. Alcoholic hepatitis (AH) is an acute and clinically distinct manifestation of alcoholic liver disease. While severe AH causes 30% or higher mortality in 3 months, treatment options are limited and ineffective. Recent advances on the understanding of the pathomechanisms of AH have identified numerous potential targets for new therapeutic interventions. Many of those targets are currently under preclinical testing and/or in human clinical trials

2017 Seminars in Liver Disease

288. The contribution of alcohol-use disorder to decompensated cirrhosis among people with hepatitis C: an international study. Full Text available with Trip Pro

The contribution of alcohol-use disorder to decompensated cirrhosis among people with hepatitis C: an international study. The advent of direct-acting antivirals (DAAs) has led to ambitious targets for hepatitis C virus (HCV) elimination. However, in the context of alcohol use disorder the ability of DAAs to achieve these targets may be compromised. The aim of this study was to evaluate the contribution of alcohol use disorder to HCV-related decompensated cirrhosis in three settings.HCV (...) benefits of DAA therapy needs to be closely monitored. Countries, where appropriate, must develop strategies combining promotion of DAA treatment uptake with management of alcohol use disorders, if World Health Organization 2030 HCV mortality reduction targets are going to be achieved.The burden of liver disease has been rising among people with hepatitis C globally. The recent introduction of highly effective medicines against hepatitis C (called direct-acting antivirals or DAAs) has brought renewed

2017 Journal of Hepatology

289. Pyroptosis by Caspase11/4-Gasdermin-D Pathway in Alcoholic Hepatitis. Full Text available with Trip Pro

Pyroptosis by Caspase11/4-Gasdermin-D Pathway in Alcoholic Hepatitis. Alcoholic hepatitis (AH) continues to be a disease with high mortality and no efficacious medical treatment. Although severe AH is presented as acute on chronic liver failure, what underlies this transition from chronic alcoholic steatohepatitis (ASH) to AH is largely unknown. To address this question, unbiased RNA sequencing and proteomic analyses were performed on livers of the recently developed AH mouse model, which (...) exhibits the shift to AH from chronic ASH upon weekly alcohol binge, and these results are compared to gene expression profiling data from AH patients. This cross-analysis has identified Casp11 (CASP4 in humans) as a commonly up-regulated gene known to be involved in the noncanonical inflammasome pathway. Immunoblotting confirms CASP11/4 activation in AH mice and patients, but not in chronic ASH mice and healthy human livers. Gasdermin-D (GSDMD), which induces pyroptosis (lytic cell death caused

2017 Hepatology

290. The circulating microbiome signature and inferred functional metagenomics in alcoholic hepatitis. Full Text available with Trip Pro

The circulating microbiome signature and inferred functional metagenomics in alcoholic hepatitis. Intestinal dysbiosis is implicated in alcoholic hepatitis (AH). However, changes in the circulating microbiome, its association with the presence and severity of AH, and its functional relevance in AH is unknown. Qualitative and quantitative assessment of changes in the circulating microbiome were performed by sequencing bacterial DNA in subjects with moderate AH (MAH) (n = 18) or severe AH (SAH (...) ) (n = 19). These data were compared with heavy drinking controls (HDCs) without obvious liver disease (n = 19) and non-alcohol-consuming controls (NACs, n = 20). The data were related to endotoxin levels and markers of monocyte activation. Linear discriminant analysis effect size (LEfSe) analysis, inferred metagenomics, and predictive functional analysis using PICRUSt were performed. There was a significant increase in 16S copies/ng DNA both in MAH (P < 0.01) and SAH (P < 0.001) subjects. Compared

2017 Hepatology

291. Challenges in the hepatic histopathology in non-alcoholic fatty liver disease Full Text available with Trip Pro

Challenges in the hepatic histopathology in non-alcoholic fatty liver disease 28159834 2018 02 26 2018 12 02 1468-3288 66 9 2017 09 Gut Gut Challenges in the hepatic histopathology in non-alcoholic fatty liver disease. 1539-1540 10.1136/gutjnl-2016-313379 Brunt Elizabeth M EM Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA. Kleiner David E DE 0000-0003-3442-4453 Laboratory of Pathology, National Cancer Institute, Bethesda, Maryland, USA (...) . eng Journal Article Research Support, N.I.H., Intramural Comment 2017 02 03 England Gut 2985108R 0017-5749 AIM IM Gut. 2017 Sep;66(9):1688-1696 27884920 Biopsy Humans Liver Non-alcoholic Fatty Liver Disease LIVER BIOPSY NONALCOHOLIC STEATOHEPATITIS Competing interests: None declared. 2016 12 29 2017 01 12 2017 01 17 2017 2 6 6 0 2018 2 27 6 0 2017 2 5 6 0 ppublish 28159834 gutjnl-2016-313379 10.1136/gutjnl-2016-313379 PMC5561367 Gut. 2017 Sep;66(9):1688-1696 27884920 Hepatology. 2011 Mar;53(3):810

2017 Gut

292. Phytosterol esters attenuate hepatic steatosis in rats with non-alcoholic fatty liver disease rats fed a high-fat diet Full Text available with Trip Pro

Phytosterol esters attenuate hepatic steatosis in rats with non-alcoholic fatty liver disease rats fed a high-fat diet Given the adverse effects of drugs used for NAFLD treatment, identifying novel and effective natural compound to prevent NAFLD is urgently needed. In the present study, the effects of phytosterol esters (PSEs) on NAFLD were explored. Adult SD rats were randomized into five groups: normal chow diet (NC), high-fat diet (HF), low-, medium- and high-dose PSE treatment plus high-fat (...) diet groups (PSEL, PSEM, and PSEH). Our results showed that the levels of LDL-C in the PSEL group and hepatic TG, TC, and FFA in the three PSEs groups were significantly decreased. Notably, the uric acid (UA) level was significantly decreased by PSEs intervention. The hepatic inflammatory stress was ameliorated via the inhibition of the cytokines, including TGF-β, IL-6, IL-10 and CRP in the PSEs intervention groups. Further, the oxidative status was improved by PSE treatment through adjusting

2017 Scientific reports

293. Branched-chain amino acids prevent hepatic fibrosis and development of hepatocellular carcinoma in a non-alcoholic steatohepatitis mouse model Full Text available with Trip Pro

Branched-chain amino acids prevent hepatic fibrosis and development of hepatocellular carcinoma in a non-alcoholic steatohepatitis mouse model Oral supplementation with branched-chain amino acids (BCAA; leucine, isoleucine, and valine) in patients with liver cirrhosis potentially suppresses the incidence of hepatocellular carcinoma (HCC) and improves event-free survival. However, the detailed mechanisms of BCAA action have not been fully elucidated. BCAA were administered to atherogenic (...) and high-fat (Ath+HF) diet-induced nonalcoholic steatohepatitis (NASH) model mice. Liver histology, tumor incidence, and gene expression profiles were evaluated. Ath+HF diet mice developed hepatic tumors at a high frequency at 68 weeks. BCAA supplementation significantly improved hepatic steatosis, inflammation, fibrosis, and tumors in Ath+HF mice at 68 weeks. GeneChip analysis demonstrated the significant resolution of pro-fibrotic gene expression by BCAA supplementation. The anti-fibrotic effect

2017 Oncotarget

294. Role of Protein Quality Control Failure in Alcoholic Hepatitis Pathogenesis Full Text available with Trip Pro

Role of Protein Quality Control Failure in Alcoholic Hepatitis Pathogenesis The mechanisms of protein quality control in hepatocytes in cases of alcoholic hepatitis (AH) including ufmylation, FAT10ylation, metacaspase 1 (Mca1), ERAD (endoplasmic reticulum-associated degradation), JUNQ (juxta nuclear quality control), IPOD (insoluble protein deposit) autophagocytosis, and ER stress are reviewed. The Mallory-Denk body (MDB) formation develops in the hepatocytes in alcoholic hepatitis

2017 Biomolecules

295. Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats Full Text available with Trip Pro

Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats The present study principally sought to investigate the effect of green tea extract (GTE) supplementation on hepatic mitochondrial DNA (mtDNA) damage in alcohol receiving rats. MtDNA was isolated from hepatic tissues of albino wistar rats after alcohol treatment with and without GTE supplementation. Entire displacement loop (D-loop) of mtDNA was screened by PCR-Sanger's sequencing (...) method. In addition, mtDNA deletions and antioxidant activity were measured in hepatic tissue of all rats. Results showed increased frequency of D-loop mutations in alcoholic rats (ALC). DNA mfold analysis predicted higher free energy for 15507C and 16116C alleles compared to their corresponding wild alleles which represents less stable secondary structures with negative impact on overall mtDNA function. Interestingly, D-loop mutations observed in ALC rats were successfully restored on GTE

2017 Journal of advanced research

296. The gamma-glutamyl transpeptidase to platelet ratio for non-invasive assessment of liver fibrosis in patients with chronic hepatitis B and non-alcoholic fatty liver disease Full Text available with Trip Pro

The gamma-glutamyl transpeptidase to platelet ratio for non-invasive assessment of liver fibrosis in patients with chronic hepatitis B and non-alcoholic fatty liver disease The gamma-glutamyl transpeptidase-to-platelet ratio (GPR) is a novel serum model, which was reported more accurate than aspartate transaminase-to-platelet ratio index (APRI) and fibrosis index based on four factors (FIB-4) for diagnosing significant fibrosis and cirrhosis in HBV mono-infection in West Africa. We aimed (...) to evaluate the diagnostic performance of GPR for liver fibrosis in patients with chronic hepatitis B (CHB) and non-alcoholic fatty liver disease (NAFLD).Of 131 patients, 41 (31.3%), 20 (15.3%), and 10 (7.6%) were classified as having significant fibrosis, severe fibrosis and cirrhosis, respectively. To predict significant fibrosis, the AUROC of GPR was higher than that of APRI (0.86 vs 0.75, p = 0.001) and FIB-4 (0.86 vs 0.66, p < 0.001). To predict severe fibrosis, the AUROC of GPR was also higher than

2017 Oncotarget

297. Coffee Drinking and Alcoholic and Nonalcoholic Fatty Liver Diseases and Viral Hepatitis in the Multiethnic Cohort Full Text available with Trip Pro

Coffee Drinking and Alcoholic and Nonalcoholic Fatty Liver Diseases and Viral Hepatitis in the Multiethnic Cohort 28300689 2018 11 13 1542-7714 15 8 2017 Aug Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association Clin. Gastroenterol. Hepatol. Coffee Drinking and Alcoholic and Nonalcoholic Fatty Liver Diseases and Viral Hepatitis in the Multiethnic Cohort. 1305-1307 S1542-3565(17)30281-1 10.1016/j.cgh.2017.02.038 Setiawan

2017 Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association

298. Perceived health and alcohol use in individuals with HIV and Hepatitis C who use drugs Full Text available with Trip Pro

Perceived health and alcohol use in individuals with HIV and Hepatitis C who use drugs Individuals who use illicit drugs are at heightened risk for HIV and/or Hepatitis C Virus (HCV). Despite the medical consequences of drinking for drug-using individuals with these infections, many do drink. In other studies, how individuals perceive their health relates to their engagement in risk behaviors such as drinking. However, among drug-using individuals with HIV and HCV, whether perceived health (...) relates to drinking is unknown.We examine the association between perceived health and drinking among drug-using individuals with HIV and/or HCV.In a large, cross-sectional study, we utilized samples of individuals with HIV (n=476), HCV (n=1145), and HIV/HCV co-infection (n=180), recruited from drug treatment centers from 2005 to 2013. In each sample, we investigated the relationship between perceived health and drinking, using ordinal logistic regressions. We present uncontrolled models as well

2017 Addictive behaviors

299. Genome-wide DNA methylation analysis during non-alcoholic steatohepatitis-related multistage hepatocarcinogenesis: comparison with hepatitis virus-related carcinogenesis Full Text available with Trip Pro

Genome-wide DNA methylation analysis during non-alcoholic steatohepatitis-related multistage hepatocarcinogenesis: comparison with hepatitis virus-related carcinogenesis The aim of this study was to clarify the significance of DNA methylation alterations during non-alcoholic steatohepatitis (NASH)-related hepatocarcinogenesis. Single-CpG-resolution genome-wide DNA methylation analysis was performed on 264 liver tissue samples using the Illumina Infinium HumanMethylation450 BeadChip. After (...) Bonferroni correction, 3331 probes showed significant DNA methylation alterations in 113 samples of non-cancerous liver tissue showing NASH (NASH-N) as compared with 55 samples of normal liver tissue (NLT). Principal component analysis using the 3331 probes revealed distinct DNA methylation profiles of NASH-N samples that were different from those of NLT samples and 37 samples of non-cancerous liver tissue showing chronic hepatitis or cirrhosis associated with hepatitis B virus (HBV) or hepatitis C virus

2017 Carcinogenesis

300. Loss of Hepatic CEACAM1: A Unifying Mechanism Linking Insulin Resistance to Obesity and Non-Alcoholic Fatty Liver Disease Full Text available with Trip Pro

Loss of Hepatic CEACAM1: A Unifying Mechanism Linking Insulin Resistance to Obesity and Non-Alcoholic Fatty Liver Disease The pathogenesis of human non-alcoholic fatty liver disease (NAFLD) remains unclear, in particular in the context of its relationship to insulin resistance and visceral obesity. Work on the carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) in mice has resolved some of the related questions. CEACAM1 promotes insulin clearance by enhancing the rate of uptake (...) of the insulin-receptor complex. It also mediates a negative acute effect of insulin on fatty acid synthase activity. This positions CEACAM1 to coordinate the regulation of insulin and lipid metabolism. Fed a regular chow diet, global null mutation of Ceacam1 manifest hyperinsulinemia, insulin resistance, obesity, and steatohepatitis. They also develop spontaneous chicken-wire fibrosis, characteristic of non-alcoholic steatohepatitis. Reduction of hepatic CEACAM1 expression plays a significant role

2017 Frontiers in endocrinology

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